title: Distinct MRI pattern in lesional and perilesional area after traumatic brain injury in rat--11 months follow-up.
abstract: To understand the dynamics of progressive brain damage after lateral fluid-percussion induced traumatic brain injury (TBI) in rat, which is the most widely used animal model of closed head TBI in humans, MRI follow-up of 11 months was performed. The evolution of tissue damage was quantified using MRI contrast parameters T(2), T(1rho), diffusion (D(av)), and tissue atrophy in the focal cortical lesion and adjacent areas: the perifocal and contralateral cortex, and the ipsilateral and contralateral hippocampus. In the primary cortical lesion area, which undergoes remarkable irreversible pathologic changes, MRI alterations start at 3 h post-injury and continue to progress for up to 6 months. In more mildly affected perifocal and hippocampal regions, the robust alterations in T(2), T(1rho), and D(av) at 3 h to 3 d post-injury normalize within the next 9-23 d, and thereafter, progressively increase for several weeks. The severity of damage in the perifocal and hippocampal areas 23 d post-injury appeared independent of the focal lesion volume. Magnetic resonance spectroscopy (MRS) performed at 5 and 10 months post-injury detected metabolic alterations in the ipsilateral hippocampus, suggesting ongoing neurodegeneration and inflammation. Our data show that TBI induced by lateral fluid-percussion injury triggers long-lasting alterations with region-dependent temporal profiles. Importantly, the temporal pattern in MRI parameters during the first 23 d post-injury can indicate the regions that will develop secondary damage. This information is valuable for targeting and timing interventions in studies aiming at alleviating or reversing the molecular and/or cellular cascades causing the delayed injury.
authors.affiliation: Biomedical NMR research group, Biomedical Imaging Unit, Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, P.O.B. 1627, FIN-70211 Kuopio, Finland.
authors.forename: Riikka J
authors.initials: RJ
authors.lastname: Immonen
authors.forename: Irina
authors.initials: I
authors.lastname: Kharatishvili
authors.forename: Juha-Pekka
authors.initials: JP
authors.lastname: Niskanen
authors.forename: Heidi
authors.initials: H
authors.lastname: Gröhn
authors.forename: Asla
authors.initials: A
authors.lastname: Pitkänen
authors.forename: Olli H J
authors.initials: OH
authors.lastname: Gröhn
mesh_terms: D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000473:pathology*; D001923:Brain Chemistry / Q000502:physiology; D001930:Brain Injuries / Q000473:pathology*; D003401:Creatine / Q000378:metabolism; D038524:Diffusion Magnetic Resonance Imaging / Q000379:methods*; D004151:Dipeptides / Q000378:metabolism; D004195:Disease Models, Animal; D005500:Follow-Up Studies; D007091:Image Processing, Computer-Assisted / Q000379:methods; D008279:Magnetic Resonance Imaging / Q000379:methods*; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D004151:Dipeptides; C027172:isospaglumic acid; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine